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[Cancer Research 37, 2348-2353, July 1, 1977]
© 1977 American Association for Cancer Research

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The Effect of Cancer on Nitrogen, Electrolyte, and Mineral Metabolism1

George L. Blackburn2, Baltej S. Maini, Bruce R. Bistrian and William V. McDermott, Jr.

Nutrition/Metabolic Laboratory, Cancer Research Institute, New England Deaconess Hospital/Harvard Medical School, Boston, and Sidney Farber Cancer Institute, Boston, Massachusetts 02215

The metabolic relationships between electrolytes, minerals, and cancer show no general abnormalities. Specific disorders of metabolism may be produced by hormonesecreting tumors, and an increased utilization or excretion of minerals and electrolytes may result. Patients with cancer and malnutrition lose significant amounts of nitrogen and fat. The attrition of visceral protein represents the most clinically significant tissue loss. The resulting nutritional conditions of marasmus and kwashiorkor account in part for the marked impairment of cell-mediated immunity. Basal energy expenditure in patients is not inordinately high, nor do different tumor groups need classification according to energy expenditure in the patients. Patients require an intake of 30 to 35 kcal/kg to meet their energy requirements. Protein intake, the most important factor in effecting weight gain, is effective when 1.5 to 2.0 g/kg are supplied daily. This represents about 16 to 20% of the total energy expenditure.

Forced feeding programs, e.g., total parenteral nutrition or enteral hyperalimentation, are often required to overcome anorexia. Response to therapy takes several weeks. A positive or successful response includes the closure of fistulae, completion of radiotherapy or chemotherapy, recovery from anorexia or stomatitis, a subjective feeling of well being, and an improvement in the quality of life. Failure to respond by these objective criteria is associated with a poor prognosis in the experience of the nutrition support service.

1 Presented at the Conference on Nutrition and Cancer Therapy, November 29 to December 1, 1976, Key Biscayne, Fla. Supported in part by NIH Research Grant GM22691. Data analysis was performed on PROPHET and was sponsored by the Chemical/Biological Information Handling Program of the Division of Research Resources, NIH (RR-76). This is Paper 586 from the Cancer Research Institute of the New England Deaconess Hospital.

2 Presenter. To whom requests for reprints should be addressed.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
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Copyright © 1977 by the American Association for Cancer Research.